The pancreas produces the hormone insulin which is secreted from specialised cells called Beta cells (β-cells) into the bloodstream in response to a rise in circulating glucose. Insulin facilitates sugar absorption from the blood into other tissues, such as the heart, muscle and fat, where it is metabolised to create energy. This process is crucial in order to regulate the body’s blood sugar level and avoid hyperglycaemia, which means there is too much glucose in the blood.
Type 2 diabetes (T2D) now affects more than 450 million people worldwide. The socioeconomic burden of the disease is substantial because it markedly increases mortality, morbidity and health care costs. T2D arises when β-cells fail to secrete adequate amounts of insulin in order to maintain blood sugar levels within a normal, healthy range. The underlying mechanism behind why this happens is not well understood.
Mitochondria are intracellular organelles which are responsible for generating energy from fuels, such as glucose. Healthy mitochondria are essential for β-cells to secrete insulin in response to a rise in blood sugar. In newly published research from the Ashcroft Group led by Postdoctoral Research Scientist Dr Elizabeth Haythorne, using a combination of techniques to examine functional, protein and gene changes, the team have found that prolonged hyperglycaemia impairs mitochondrial metabolism and energy production. They also found that multiple genes and proteins involved in the metabolic pathways glycolysis and gluconeogenesis were abnormally upregulated.
These sets of data indicate that hyperglycaemia induces a significant dysregulation of major metabolic pathways in pancreatic β-cells. The researchers propose that this underlies the progressive failure of β-cells in diabetes.
The full publication Diabetes causes marked inhibition of mitochondrial metabolism in pancreatic β-cells is available to read here.